Takotsubo Syndrome (TTS) –also known as Takotsubo Cardiomyopathy, stress-induced cardiomyopathy, transient apical ballooning, and broken heart syndrome –is a condition that is generally triggered by emotional or physical stress and is characterized by transient regional left ventricular (LV) systolic dysfunction. First described in Japan, the term Takotsubo is derived from the Japanese word meaning octopus trap due to the characteristic apical ballooning appearance of the left ventricle. About 2 % of the patients presenting with acute myocardial syndrome have TTS.1 Clinically, individuals present with chest pain, electrocardiographic changes, troponin elevation, and left ventricular dysfunction mimicking acute myocardial infarction without the presence of obstructive coronary artery disease or plaque rupture. In most cases, the regional wall motion abnormality extends beyond one territory and is not limited to a single epicardial coronary artery.2

Chronic kidney disease (CKD) is a progressive condition characterized by structural and functional changes to the kidney due to various etiologies. CKD is typically defined as a reduction in kidney function, an estimated glomerular filtration rate (eGFR) of <60 mL/min per 1·73 m2, or markers of kidney damage, such as albuminuria, hematuria, or abnormalities detected through laboratory testing or imaging and that are present for at least 3 months. The global burden of CKD is substantial and growing: approximately 10 % of adults worldwide are affected by some form of the disease, which results in 1·2 million deaths and 28 million years of life lost each year. By 2040, CKD is estimated to become the fifth leading cause of death globally—one of the largest projected increases of any major cause of death.3

CKD patients have a considerably higher mortality risk than age-matched controls, and renal dysfunction is an independent predictor of adverse outcomes among heart failure patients.4 Patients with end-stage renal disease are also exposed to many stressors such as volume overload, abrupt changes in hemodynamic and metabolic states, and myocardial stunning during dialysis, that may lead to acute exaggerated sympathetic nervous activity, including local renal and cardiac sympathetic over-activation. Even non-dialytic CKD is associated with sympathetic overactivity, thereby being one of the major comorbidities associated with TTS.5

This review aims to consolidate our current understanding to describe the prevalence and impact of chronic kidney disease on outcomes and recurrence of TTS, in addition to discussing pathophysiological mechanisms, clinical implications, and management.